The in vitro effect of triamcinolone acetonide on branching morphogenesis in the fetal rat lung

1992 ◽  
Vol 14 (1) ◽  
pp. 28-36 ◽  
Author(s):  
Emad A. S. Massoud ◽  
Harmanjatinder S. Sekhon ◽  
Avi Rotschild ◽  
William M. Thurlbeck
1993 ◽  
Vol 15 (2) ◽  
pp. 89-97 ◽  
Author(s):  
Emad A. S. Massoud ◽  
Harmanjatinder S. Sekhon ◽  
Avi Rotschild ◽  
Martin L. Puterman ◽  
Reiko Matsui ◽  
...  

2000 ◽  
Vol 278 (5) ◽  
pp. L1062-L1070 ◽  
Author(s):  
B. Keith Taylor ◽  
Tamara D. Stoops ◽  
Allen D. Everett

Protein phosphatase 2A (PP2A) is a key signal transduction intermediate in the regulation of cellular proliferation and differentiation in vitro. However, the role of PP2A in the context of a developing organ is unknown. To explore the role of PP2A in the regulation of lung development, we studied the effect of PP2A inhibition on new airway branching, induction of apoptosis, DNA synthesis, and expression of epithelial marker genes in whole organ explant cultures of embryonic (E14) rat lung. Microdissected lung primordia were cultured in medium containing one of either two PP2A inhibitors, okadaic acid (OA, 0–9 nM) or cantharidin (Can, 0–3,600 nM), or with the PP2B inhibitor deltamethrin (Del, 0–10 μM) as a control for a PP2A-specific effect for 48 h. PP2A inhibition with OA and Can significantly inhibited airway branching and overall lung growth. PP2B inhibition with Del did not affect lung growth or new airway development. Histologically, both PP2A- and PP2B-inhibited explants were similar to controls. Increased apoptosis was not the mechanism of decreased lung growth and new airway branching inasmuch as OA-treated explant sections subjected to the terminal deoxynucleotidyltransferase dUTP nick end labeling reaction demonstrated a decrease in apoptosis. However, PP2A inhibition with OA increased DNA content and 5-bromo-2′-deoxyuridine uptake that correlated with a G2/M cell cycle arrest. PP2A inhibition also resulted in altered differentiation of the respiratory epithelium as evidenced by decreased mRNA levels of the early epithelial marker surfactant protein C. These findings suggest that inhibition of protein phosphatases with OA and Can halted mesenchymal cell cycle progression and reduced branching morphogenesis in fetal rat lung explant culture.


2013 ◽  
Vol 03 (01) ◽  
pp. 4-12 ◽  
Author(s):  
Asra Ahmed ◽  
James A. Thliveris ◽  
Anthony Shaw ◽  
Michael Sowa ◽  
James Gilchrist ◽  
...  

1986 ◽  
Vol 20 (5) ◽  
pp. 473-477 ◽  
Author(s):  
Lan Gross ◽  
Diane W Dynia ◽  
Seamus A Rooney ◽  
Douglas A Smart ◽  
Joseph B Warshaw ◽  
...  

2002 ◽  
Vol 282 (3) ◽  
pp. L379-L385 ◽  
Author(s):  
Stephen L. Young ◽  
Katherine Evans ◽  
Jerry P. Eu

Cells of the developing lung express the constitutive nitric oxide synthases (NOSs) I and III. The developmental importance of these enzymes is largely unknown, although a role for nitric oxide (NO) in the regulation of pulmonary blood flow at birth is established. Known effects of NO on transcription factors, apoptosis, and cellular proliferation, plus the time and spatial limits of pulmonary NOS expression, suggest that NO might influence lung development. We tested the potential of NO to modulate lung branching morphogenesis by exposing lung explants from gestational day 13 rat fetuses to varying doses of several NO donors (NONO-ate). We counted the number of airway branches that were added between the first and 72nd h of culture. NO released only from a NONO-ate with a long half-life {( Z)-1-[2-(2-aminoethyl)- N-(2-ammonioethyl)amino]-diazen-1-ium-1,2-diolate-NO}, increased branching in ambient O2 by twofold. The NO effect was not mimicked with a cyclic guanine monophosphate analog; nonspecific NOS inhibitors in millimolar concentrations inhibited branching. We conclude that endogenous and exogenous NO can modulate branching morphogenesis in the rat lung.


1978 ◽  
Vol 45 (3) ◽  
pp. 355-362 ◽  
Author(s):  
I. Gross ◽  
G. J. Smith ◽  
W. M. Maniscalco ◽  
M. R. Czajka ◽  
C. M. Wilson ◽  
...  

We have developed a short-term organ culture model for the study of the biochemical and morphological development of late gestation fetal rat lung. Explants (1 mm3) of 19-day lung were cultured in an oxygen enriched environment in the presence of synthetic serum-free medium for 3 days. Morphological maturation continued in culture. The rate of incorporation of choline into disaturated phosphatidylcholine and the content of this phospholipid in the explants increased in vitro in a pattern very similar to that which occurs in vivo. The activities of choline kinase and cholinephosphotransferase were also similar in cultured lung and in vivo. Studies of glucose oxidation to CO2 provided additional evidence that the explants remained viable in culture. The explants retained the sensitivity of fetal lung to hormonal action. This was demonstrated by the stimulation of choline incorporation into phospholipid by cyclic AMP and an increase in the glycogen content after exposure to insulin.


1987 ◽  
Vol 12 (3) ◽  
pp. 253-264 ◽  
Author(s):  
Stephen J. M. Skinner ◽  
Martin Post ◽  
John S. Torday ◽  
Alan D. Stiles ◽  
Barry T. Smith
Keyword(s):  
Type Ii ◽  
Rat Lung ◽  

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